Does neutral evolution explain the genetic differences between humans and chimpanzees

John still has to learn the difference between evolutionary competition and evolutionary adaptation. Competition depends on the relative fitnesses of the different variants while evolutionary adaptation depends on the ability of a variant to replicate. The reason for that is that for any chance of a beneficial mutation to occur, it has to occur at replication. Study and understand the similarities and differences of the Kishony and Lenski experiments to see how the process of evolutionary competition and evolutionary adaptation operate.

That depends on the local environment and how close the population is to a local fitness maximum. The closer the population is to the fitness maximum the less chance it will have a mutation to increase fitness - if youā€™re near the top of the mountain already there are few ways to climb higher. However in the real world environments are constantly changing and reproductive fitness maxima are always moving. The process of evolution allows the population to constantly track and move toward the local fitness maximum. Asking for a specific number of beneficial mutations is rather silly as there are way too many variables in the equations to calculate.

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That would depend on the probability of a beneficial mutation occurring. Which is a difficult thing to estimate, as most experimental tests of the question only address ā€˜beneficial in a specific artificial environmentā€™, rather than any possible beneficial mutation. And ignores the fact that mutations without any adaptive effect in one environment may be beneficial in another.

Still, I doubt the rate of beneficial mutations is any lower than 1 every 10k generations or so, since the experimental values are higher in nearly every experiment Iā€™m familiar with. So if ā€˜reasonable probabilityā€™ means 5%, then 500-600 generations. If it means 95%, then ~30k generations. ~280k generations since the most recent common ancestor with chimpanzees, so Iā€™d say the probability of at least one beneficial mutation is really good.

If you disagree, andā€¦

ā€¦let me know.

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Sure neutral evolution exists but to assume that neutral evolution accounts for all the genetic differences between humans and chimpanzees does not explain why humans have achieved far larger populations than chimps have. If humans and chimpanzees evolved from a common ancestor, and the only genetic differences between the two replicators are neutral mutations, why have humans achieved such a vastly larger population? Explain that logic. Shouldnā€™t the human lineage have gotten one or more beneficial mutations? If so, how many replications required for a reasonable probability of those beneficial mutations occurring. Iā€™ll even give you a hint, doubling population size does not double the probability of a beneficial mutation occurring.

That seems even more like word salad than usual for you. Why does a beneficial mutation have to occur at replication rather than as a result of lesion or repair? Why should that determine what counts as adaptation?

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Yes, that is true, and entirely beside the point.

The case I made for CD only requires that most mutations are evolving largely neutrally. Certainly some are not neutral mutations, but that is just a small fraction of fixed mutations.

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Nobody assumes that neutral evolution accounts for all the differences, just most of them, and the discussion is about the rule, not the rare exceptions.

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Itā€™s not too hard to calculate. Letā€™s say you have a mutation rate of 1e-9. How many replications are required for you to have at least one of those descendent in that population have a mutation at one of every possible site in the genome? Then, how many replications required to have at least one of those descendants in that population to have every possible base substitution in that genome. For a visual hint, watch the Kishony experiment video.

You donā€™t compute that probability based on generations alone. It depends on the number of replications of the particular variant each generation. The probability of a beneficial mutation occurring must be computed by using the summation of replications over generations, The replication is one of the random trials in DNA evolution. The other random trial is the mutation itself which can have multiple possible outcomes including a base substitution, deletion, insertion, double deletion, double insertionā€¦ Hereā€™s a paper that shows you how to do this math:
The basic science and mathematics of random mutation and natural selection
This paper also explains the mathematical behavior of the Kishony experiment.

He didnā€™t say all mutations were neutral. He said the large majority of mutations are neutral which they are. I already explained above why a relatively small number of beneficial mutations led to a very large increase in human population.

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The mutation has to occur in a germ cell line or gamete, not in a somatic cell.

Tell us how many mutations need to be beneficial to account for that difference. Since @swamidass said ā€˜mostā€™ and you are arguing against that ā€˜mostā€™, your claim so far as I can tell is that ~10m mutations (~half the fixed differences) are beneficial. That sounds insane. If that isnā€™t your claim (as I hope it isnā€™t), then you need to do a better job explaining 1) what your claim actually is and 2) why it is in contradiction with @swamidassā€™s claim.

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Adaptation does not require fixed mutations, but at least you are starting to get the point that something beyond neutral mutations have occurred for humans and chimps to have come from a common ancestor. Now you need to learn what it takes for a lineage to accumulate one or more beneficial mutations. You should start by studying the Kishony and Lenski experiments. In the Kishony experiment, adaptation occurs without fixation of any mutation. On the other hand, fixation is required for adaptation in the Lenski experiment. Why do you think that happens?

You understand that this is quite different from your original statement, right? And do you also understand that you have unaccountably switched the subject from single-celled organisms to multicellular ones without vegetative reproduction?

That would be half of the half, ~20m, attributed to the human lineage, since there are around 40 million fixed differences.

I see that Kleinman, as usual, only briefly referenced the supposed subject as an excuse to go on about his obsession.

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What were those relatively small number of beneficial mutations that did that? Letā€™s say it was 5 particular mutations necessary to give that improvement in fitness of humans over chimpanzees. How does a lineage of humans accumulate those 5 particular beneficial mutations? Iā€™ll give you a hint, it depends on the mutation rate and the number of replications for each variant at each evolutionary adaptive step.

I call Texas Sharpshooter.

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Yes, you do calculate the probability of a mutation occurring in a lineage by the mutation rate and the number of generations. What are you actually trying to say, and why do you insist on using nonstandard language to say it?

I ā€˜thinkā€™ thatā€™s what heā€™s talking about. It is hard to say, because he refuses to define his terms or use standard language. I mean look at this:

Pure word-salad nonsense.

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In parallel, not in sequence :slight_smile: .

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Hereā€™s how evolution works in parallel and it works orders of magnitude more slowly that in sequence.
The mathematics of random mutation and natural selection for multiple simultaneous selection pressures and the evolution of antimicrobial drug resistance
This paper explains why it takes 3 drugs to give a durable treatment of HIV and why it when Kishony tried to run his experiment with 2 drugs, it didnā€™t work. Do you understand the mathematical reason for this?

It wouldnā€™t have anything to do with linkage and recombination? It appears that you are viewing humans as haploid organisms.

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